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The ability of HIV to mutate and rapidly evolve to escape immune detection by the most-prevalent HLA molecules is similar to the rapid adaptation and mutation of other infectious viruses, such as influenza.
Although Ser 215 is the dominant and common site responsible for phosphorylation of TTG1 by SK11 and SK12, other sites may also contribute to TTG1 phosphorylation since mutation of other sites slightly alters the overall phosphorylation patterns mediated by SK11 and SK12 (Fig. 4c, d).
Subsequent discoveries of additional thermostable polymerases and the mutation of other enzymes in the polymerase family has enabled the development of high fidelity, long read polymerases, all of which have added to the robustness of the PCR technique.
Prior to that it has already been shown that mutation of Ser57 and His355 completely abolished the enzymatic activity of HEF, essentially confirming the data from crystallography, but mutation of other residues in the vicinity, i.e. Asp247, Asn266 and His354 also affected the hydrolytic activity of HEF (Pleschka et al., 1995).
Mutation of other W residues had no effect on the processing and targeting into lysosome, as shown by W307L mutant.
Mutation of other reported S/T*-P sites in raptor did not collapse the bandshift (Fig. 3a, data not shown).
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Sequential studies showed that the original ASXL1 mutation remained unchanged at disease progression in all 32 ASXL1-mutated patients but were frequently accompanied with acquisition of mutations of other genes, including RUNX1, NRAS, KRAS, SF3B1, SETBP1 and chromosomal evolution.
However, generally targeted therapies are only cytostatic and a proportion of the patient population may be non-responsive to targeted therapy due to mutations of other genes in the same pathway (e.g. ras mutations in patients with colorectal cancer treated with EGFR targeted therapy).
In order to better understand the role of those mutations in disturbing normal channel functions on a structural level, we mapped the disease-related mutations of other human Nav channels onto the Nav1.7 structure model based on the sequence alignment reported in Wu et al., 2016 (Fig. 3).
On the contrary, mutations of other residues in this second group reduce not only the kinase activity but also the epimerase activity of the full length protein ([11], Table 1).
Activating somatic mutations of other oncogenes (EGFR, KRAS, HRAS, NRAF, BRAF and AKT1) involved in downstream molecular events following tyrosine kinase receptor activation are frequent in several malignancies but rare in breast cancer.
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